Year: 2026
Type: editorial
Abstract: Welcome to the latest issue of “Seminars in Thrombosis and Hemostasis (STH)” published under the “banner” of “Editorial Compilation,” this being the 18th such issue ([ Table 1 ]). Historically, “STH” is a theme-driven publication; however, ongoing opportunities emerge to disseminate wide-ranging contributions of current interest or controversy, which do not directly suit an ongoing themed issue. We also require a medium to enable publication of peer-reviewed “unsolicited” manuscripts if accepted, as well as contributions from our Eberhard F. Mammen Young Investigator Award winners (see [ Table 2 ] for previous Editorials related to the Eberhard F. Mammen awards). As is now standard for this compilation series, this study contains a mixture of articles that comprise the above elements, as well as broadly fitting within the standard themes of “thrombosis” and “bleeding.” Table 1 Past STH issues in the series “editorial compilation” 1. Favaloro EJ, Lippi G. Editorial compilation I. Semin Thromb Hemost. 2016 Feb;42(1):5–8 2. Favaloro EJ, Lippi G. Editorial compilation II. Semin Thromb Hemost. 2016 Sep;42(6):599–602 3. Favaloro EJ, Lippi G. Editorial compilation III. Semin Thromb Hemost. 2017 Feb;43(1):4–7 4. Favaloro EJ, Lippi G. Editorial compilation IV. Semin Thromb Hemost. 2017 Sep;43(6):549–552 5. Favaloro EJ, Lippi G. Editorial compilation V. Semin Thromb Hemost. 2018 Apr;44(3):193–196 6. Favaloro EJ, Lippi G. Editorial compilation VI. Semin Thromb Hemost. 2019 Feb;45(1):5–9 7. Favaloro EJ, Lippi G. Editorial compilation VII. Semin Thromb Hemost. 2019 Jul;45(5):429–432 8. Favaloro EJ, Lippi G. Editorial compilation VIII. Semin Thromb Hemost. 2020 Jun;46(4):393–397 9. Favaloro EJ, Lippi G. Editorial compilation IX. Semin Thromb Hemost. 2021 Feb;47(1):6–10 10. Favaloro EJ, Lippi G. Editorial compilation X. Semin Thromb Hemost. 2021 Oct 47(7):754–758 11. Favaloro EJ, Lippi G. Editorial compilation XI. Semin Thromb Hemost. 2022 Mar;48(2):127–131 12. Favaloro EJ, Pasalic L, Lippi G. Editorial compilation XII. Semin Thromb Hemost. 2022 Jul;48(5):497–501 13. Favaloro EJ, Pasalic L, Lippi G. Editorial compilation XIII. Semin Thromb Hemost. 2023 Jul;49(5):427–432 14. Favaloro EJ, Pasalic L, Lippi G. Editorial compilation XIV. Semin Thromb Hemost. 2024 Mar; 50(2):151–156 15. Favaloro EJ, Pasalic L, Lippi G. Editorial compilation-XV. Semin Thromb Hemost. 2024 Jun;50(4):521–526 16. Vu HH, McCarty OJT, Favaloro EJ. Contact activation: where thrombosis and hemostasis meet on a foreign surface, plus a mini-editorial compilation (“part XVI”). Semin Thromb Hemost. 2024 Oct;50(7):933–936 17. Favaloro EJ, Pasalic L, Fan BE, Lippi G. Editorial compilation-XVII. Semin Thromb Hemost. 2025 Jun;51(5):475–480 Table 2 Past STH editorials related to Eberhard F. Mammen award announcements 1. Favaloro EJ. Welcome to a special issue of Seminars in Thrombosis and Hemostasis—the closing issue for 2008. Semin Thromb Hemost 2008; 34: 693–696 2. Favaloro EJ. A Tribute to Eberhard F. Mammen, M.D. (1930–2008). Semin Thromb Hemost 2008; 34: 703–708 3. Favaloro EJ. Welcome to the first issue of Seminars in Thrombosis and Hemostasis for 2009. Semin Thromb Hemost 2009; 35:1–2 4. Favaloro EJ. Winners of the Inaugural Eberhard F. Mammen Award for most popular article. Semin Thromb Hemost 2009; 35: 587–590 5. Favaloro EJ. Editorial. 2009 Eberhard F. Mammen Young Investigator Award Winners. Semin Thromb Hemost 2010; 36: 469–470 6. Favaloro EJ. Winners of the 2010 Eberhard F. Mammen award for most popular article during 2008–2009. Semin Thromb Hemost. 2010;36(7):685–692 7. Favaloro EJ. 2011 Eberhard F. Mammen award announcements. Semin Thromb Hemost. 2011;37(5):431–439 8. Favaloro EJ. 2012 Eberhard F. Mammen award announcements. Semin Thromb Hemost. 2012;38:425–432 9. Favaloro EJ. 2013 Eberhard F. Mammen award announcements. Semin Thromb Hemost. 39:567–574 10. Favaloro EJ. 2014 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2014;40(4):407–412 11. Favaloro EJ. 2014 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2014;40(7):718–723 12. Favaloro EJ. 2015 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2015;41(7):673–679 13. Favaloro EJ. 2015 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2015;41(8):809–815 14. Favaloro EJ. 2016 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2016;42(4):325–330 15. Favaloro EJ. 2016 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2017;43(3):235–241 16. Favaloro EJ. 2017 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2017;43(4):357–363 17. Favaloro EJ. 2017 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2018;44(2):81–88 18. Favaloro EJ. 2018 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2018;44(3):185–192 19. Favaloro EJ. 2018 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2019;45(2):123–129 20. Favaloro EJ. 2019 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2019;45(3):215–224 21. Favaloro EJ. 2019 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost 2020;46(2):105–113 22. Favaloro EJ. 2020 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2020;46(4):383–392 23. Favaloro EJ. 2020 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost 2021;46(3): 229–237 24. Favaloro EJ. 2021 Eberhard F. Mammen Award Announcements: Part I—Most Popular Articles. Semin Thromb Hemost. 2021 Jul;47(5):467–476 25. Favaloro EJ. 2021 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2022 Apr;48(3):265–273 26. Favaloro EJ. 2022 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2022 Jul;48(5):502–513 27. Favaloro EJ. 2023 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2023 Jul;49(5):417–426 28. Favaloro EJ. 2022 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2023 Nov;49(8):775–782 29. Favaloro EJ. 2024 Eberhard F. Mammen award announcements: part I—most popular articles. Semin Thromb Hemost. 2024 Oct;50(7):919–932 30. Favaloro EJ. 2023 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2024 Nov;50(8):1049–1057 31. Favaloro EJ. 2024 Eberhard F. Mammen award announcements: part II—young investigator awards. Semin Thromb Hemost. 2025 Jun;51(5):481–449 This issue begins with a review on disseminated intravascular coagulation (DIC) by Iba et al,[ 1 ] who introduce the readers of STH to the new definition and diagnostic criteria recently released by the International Society on Thrombosis and Haemostasis. The new guidance reflects advances in understanding the pathophysiology of DIC, which is now defined as an acquired, life-threatening condition involving systemic coagulation activation, impaired fibrinolysis, and endothelial injury. The revised framework emphasizes the condition's dynamic nature, progressing from preclinical abnormalities to overt clinical manifestations such as bleeding and (multiple) organ dysfunction. A major innovation in the 2025 update is the phase-based classification of DIC: pre-DIC, early phase DIC, and overt DIC. Early phase DIC—also referred to as subclinical or compensated DIC—is characterized by laboratory abnormalities preceding clinical symptoms. Overt DIC represents the advanced stage with clear evidence of coagulopathy and organ failure. Importantly, the new criteria are tailored to the underlying disease, such as sepsis, trauma, or malignancy. For example, the sepsis-induced coagulopathy score is now acknowledged as a tool for detecting early-phase DIC in septic patients. The overt DIC scoring system has been refined, including revised D-dimer thresholds: levels >3× and >7× the upper normal limit now corresponding to 2 and 3 points, respectively. Platelet count, prothrombin time-International Normalized Ratio, and fibrinogen levels remain key indicators. The criteria also classify DIC into thrombotic and hemorrhagic phenotypes. Thrombotic DIC is marked by microvascular thrombosis and organ dysfunction, while hemorrhagic DIC is characterized by bleeding due to consumption of coagulation factors. By introducing clearer definitions and individualized approaches, these updates aim to enable earlier diagnosis and more effective management of DIC across clinical contexts. Next, Østergaard et al explore the mechanisms of hypercoagulability in thrombotic antiphospholipid syndrome (APS) with a focus on human studies.[ 2 ] Thrombosis is the most common manifestation of APS, but concurring evidence of the mechanisms leading to a hypercoagulable state and thereby thrombosis is lacking. Existing reviews on this topic often include both animal and in vitro models. Additionally, studies with a systematic approach and stringent methodology, focusing exclusively on human studies, are lacking. Therefore, the authors conducted a scoping review of studies with human subjects, focusing on the mechanisms contributing to hypercoagulability in thrombotic APS (TAPS). The process was guided by the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) Extension for Scoping Reviews and performed according to a preregistered protocol in Open Science Framework. A systematic search of Ovid (EMBASE) and MEDLINE (PubMed) was performed. Records investigating mechanisms of hypercoagulability in adults (≥18 years) with TAPS, published between January 2000 and October 2024, were included. A total of 4,160 titles and abstracts were screened, 115 articles were assessed in full text, of which 35 studies fulfilled the predefined eligibility criteria for inclusion. Of the included studies, eight focused on primary hemostasis, 10 on secondary hemostasis, nine on fibrinolysis, four on neutrophil extracellular traps (NETs), six on endothelial cells, three on complement factors, five on monocytes, three on oxidized low-density lipoprotein complexes, two on oxidative stress, and one on amyloid-β1–40. No clear consensus was found regarding the underlying cause of hypercoagulability in TAPS, highlighting the need for further studies with human subjects. Nonetheless, the scoping review indicates that hypercoagulability in TAPS is possibly multifactorial, with no single mechanism being solely responsible. This issue of STH continues with a review on the risks and benefits of nonsteroidal anti-inflammatory drugs (NSAIDs) in the hemostatic system by Cignarella et al.[ 3 ] Chronic use of multiple drugs increases the risk of adverse drug reactions, drug interactions, and poor therapeutic adherence. In elderly or frail patients, some drugs may become ineffective or even harmful with advancing age and worsening clinical conditions. NSAIDs have been extensively used for decades and, as a class, are often inappropriately prescribed and involved in polypharmacotherapy, with untoward effects. In view of the dynamic and mutual relationship between inflammation and hemostasis in various clinical scenarios, the use of anti-inflammatory agents, including NSAIDs, may tip this difficult balance in patients with hemostatic disorders. Rather than on well-established actions such as the clinically relevant antiplatelet action of low-dose aspirin and gastrointestinal bleeding, this review focuses on less highlighted, emerging, or sometimes overlooked NSAID efficacy and safety endpoints. For instance, preclinical studies suggest that the antiplatelet action of low-dose aspirin enhances immune system activity against cancer cells, thereby preventing metastasis. While use of NSAIDs in patients with coagulation disorders may have an acceptable risk-to-benefit ratio in selected patients, clinical judgement is required, especially in cases of renal impairment that can be worsened by NSAIDs or in cases with high bleeding risk, such as in hemophilia. In the context of polypharmacotherapy, attenuation of aspirin antiplatelet action by concomitant and inaccurately timed ibuprofen treatment may undermine the clinical benefit of aspirin in cardiovascular prevention. Thus, collaborative cross-disciplinary efforts of pharmacologists and clinicians would be desirable to enhance appropriateness, efficacy, and safety of NSAID treatment in different settings of care. Next, Petrou et al review the ABO blood system in relation to hemostasis and thrombosis.[ 4 ] The relationship between non-O blood groups and thromboembolic events has been suggested by several studies, although the exact underlying mechanisms are not fully elucidated. However, the correlation between ABO blood groups with the opposite pole of hemostasis, hemorrhage, has been investigated less thoroughly. Non-O blood groups confer an overall increased risk of single, recurrent, and provoked thromboembolic episodes. On the other hand, blood group O has been associated with more severe bleeding events and less favorable manifestations in individuals with hemorrhagic disorders. Therefore, ABO blood group screening may play a role in assessing both thrombotic and hemorrhagic risks and could potentially be incorporated into existing clinical prediction systems. This strong belief is supported by the ongoing research. Nevertheless, to date, the majority of studies exhibit significant heterogeneity, and given the prevalence of non-O blood groups, a natural reluctance to incorporate blood groups into risk assessment models arises. Therefore, a more targeted approach should be considered to provide safe outcomes. The in vitro estimation of the thrombotic and hemorrhagic profile of each blood group separately, the quantitative estimation of von Willebrand factor and factor VIII level and activity, together with platelet function in several disease settings and in well-organized studies, could be useful to establish a clear relationship of ABO blood types with hemostatic and thrombotic disorders. This approach ensures a safe method for categorizing a patient's risk, managing treatment, and influencing prognosis. Sokou et al then review platelet and plasma transfusion strategies for neonates, assessing the evidence, guidelines, and addressing unanswered questions.[ 5 ] The transfusion of platelets and fresh frozen plasma (FFP) to critically ill neonates in neonatal intensive care units is a common intervention, yet it is still widely performed without adhering to international guidelines. The guidance itself on the therapeutic management of neonatal coagulation disorders is generally limited due to the absence of strong indications for treatment and is mainly aimed at preventing major hemorrhagic events, such as intraventricular hemorrhage in premature neonates. Historically, the under-representation of neonates in clinical studies related to transfusion medicine has led to significant gaps in knowledge regarding the best transfusion practices in this vulnerable group and to a wide variability in policies among different neonatal units, often based on local experience or guidance designed for older children or adults, and possibly increasing the risk of inappropriate or ineffective interventions. Platelet transfusion and, in particular, FFP administration have been linked to potentially fatal complications in neonates, so that any decision needs to be carefully balanced and requires a thorough consideration of multiple factors in the neonatal population. Despite recent advances toward more restrictive practices, platelet and FFP transfusions are still subject to wide variability in practice. A review on neutrophils and NETs is then presented by Hassani et al.[ 6 ] The authors remind us that neutrophils are astonishing cells involved in nonspecific immunity, especially against bacterial and fungal infections. Their half-life is short, but despite their important role in nonspecific immunity, they defend the host even after their death by providing secondary structures such as NETs, which reflect a network comprising DNA, histones, and proteins, including elastase, cathepsin G, and myeloperoxidase. In this context, in addition to their primary role in hemostasis, NETs also play a role in thrombosis, an area that has perhaps received less attention. Nonetheless, NETs can promote both venous and arterial thrombus formation (immuno-thrombosis) by their effects on primary and secondary hemostasis. Their participation in thrombus formation includes the release of microparticles and components of the inflammasome. Neutrophils, in interaction with other cells, including platelets, can further contribute to thrombosis. Activated platelets can capture neutrophil-derived microparticles containing tissue factor (TF), leading to TF accumulation and increased fibrin deposition. Furthermore, neutrophil inflammasomes, as a regulator of the generation of IL-1 family proteins, have been shown to boost thrombosis formation in response to hypoxia. Overall, understanding the complex and reciprocal effects of neutrophils with other hemostasis-related cells and components provides important insights into hemostatic mechanisms, and this may open avenues in medical research and potential therapeutic interventions. The review by Huang et al[ 7 ] is also focused on NETS, but this time in relation to their use as a strategy for treating acute ischemic stroke (AIS) based on thrombolysis resistance. AIS is a life-threatening thrombotic disorder, with intravenous thrombolysis serving as the first-line treatment during its acute phase. However, thrombolysis resistance diminishes the success rate of early reperfusion. Recent studies have highlighted NETs as a critical factor contributing to thrombolysis resistance. Targeting NETs with deoxyribonuclease I has been shown to significantly improve the thrombolytic efficacy of recombinant tissue plasminogen activator and reduce the risk of hemorrhagic transformation. In this review, the authors summarize current knowledge on the mechanisms by which NETs contribute to thrombosis and thrombolysis resistance, explore the prospective and feasibility of targeting NETs to improve thrombolysis, and provide information about the creation of innovative thrombolytic treatment approaches for AIS. The last review in this issue of STH is by Kalantari et al, who review thrombocytopenia after hematopoietic stem cell transplantation (HSCT) in both pediatric and adult patients.[ 8 ] Thrombocytopenia following HSCT is a common complication that is associated with a remarkable increase in morbidity and mortality. Post-HSCT thrombocytopenia is a multifactorial condition with several mechanisms, including reduced platelet in platelet and disease, and mechanisms are potential risk factors for of thrombocytopenia focuses on care platelet are used to and complement are treatment with and effects. However, further research is for treatment and care. 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DOI: 10.1055/a-2741-8146
Authors: Emmanuel J. Favaloro, Leonardo Pasalic, Bingwen E. Fan, Giuseppe Lippi
Language: English
Subfield: Hematology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W7123649654